Surgery
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Resuscitated hemorrhagic shock predisposes patients to the development of organ dysfunction, particularly to lung injury. Ischemia/reperfusion during shock is believed to prime the immune system for an exaggerated inflammatory response to a second delayed stimulus. We previously reported an in vitro model of oxidant-induced priming of the macrophage to lipopolysaccharide (LPS) involves the Src family of tyrosine kinases. Because the Src family has been shown to activate the p38 mitogen-activated protein kinase (MAPK) pathway, we hypothesize that LPS signaling after oxidant stress involves the p38 pathway and is activated by Src kinases. ⋯ Oxidant stress generated during global ischemia/reperfusion activates p38 MAPK in an Src-dependent manner. Oxidants seem to alter the LPS-induced activation of p38. P38 does not seem to have a direct role in leading to oxidant-induced NF-kappaB translocation but may affect other oxidant-induced transcription factors. This altered pathway provides an alternative avenue to target therapy during the oxidant-induced priming of the macrophage induced by trauma resuscitation.
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Heme oxygenase (HO)-1 system has been shown to provide protection against oxidative stress through the degradation of heme to biliverdin, free iron, and carbon monoxide (CO). This study investigated cytoprotective efficacy of CO at a low concentration on cold ischemia/reperfusion (I/R) injury of transplanted intestine. ⋯ These results indicate a significant role for CO in protecting the intestine from cold I/R injury associating with small intestinal transplantation.
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Resuscitated hemorrhagic shock predisposes patients to the development of acute respiratory distress syndrome (ARDS). Hypertonic saline (HTS) has been shown to inhibit immune cell activation in response to lipopolysaccharide (LPS) in vitro and to reduce lung damage when used for resuscitation of hemorrhagic shock in vivo. We hypothesize that HTS resuscitation of hemorrhagic shock may exert this anti-inflammatory effect by modulating alveolar macrophage function leading to an altered balance between the proinflammatory and the counter-inflammatory response. ⋯ HTS resuscitation exerts an immunomodulatory effect on alveolar macrophages by shifting the balance of pro- and counter-inflammatory cytokine production in favor of an anti-inflammatory response. The in vivo data suggest a causal role for HTS-induced augmented IL-10 as protective. These findings suggest a novel mechanism for the in vivo salutary effect of HTS resuscitation on lung injury after resuscitated hemorrhagic shock.
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Randomized controlled trials (RCTs) are considered the gold standard for evidence-based clinical research, but prior work has suggested that there may be poor reporting of sample sizes in the surgical literature. Sample size calculations are essential for planning a study to minimize both type I and type II errors. We hypothesized that sample size calculations may not be performed consistently in surgery studies and, therefore, many studies may be "underpowered." To address this issue, we reviewed RCTs published in the surgical literature to determine how often sample size calculations were reported and to analyze each study's ability to detect varying degrees of differences in outcomes. ⋯ The reporting of sample size calculations was not provided in more than 60% of recently published surgical RCTs. Moreover, only half of studies had sample sizes appropriate to detect large differences between treatment groups.
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The hypothesis of this study was that differences exist among patients with private insurance compared with patients with Medicaid or no insurance, regarding access to the timely treatment of abdominal aortic aneurysms (AAAs) and the outcomes of AAA repair. ⋯ Uninsured patients more often seek treatment of ruptured AAAs compared with patients with private insurance. Operative mortality rates in uninsured patients are greater for elective and emergent AAA repair. These data support the tenet that payer status is associated with mortality rates after AAA repair.